Hôpitaux Universitaires de Strasbourg Strasbourg, France
Correspondence to: Emmanuel Andrès, MD, Service de Médecine Interne, Clinique Médicale B, Hôpital Civil, Hôpitaux Universitaires de Strasbourg, 1 place de l’Hôpital à 67 091 Strasbourg Cedex, France; e-mail: firstname.lastname@example.org
We read with great interest the article of Caldera et al1
about pulmonary embolism in a patient with pernicious anemia and hyperhomocysteinemia (October 2002). This case report illustrates the potential role of a cobalamin deficiency, here related to pernicious anemia, in the pathogenesis of venous thrombosis, especially in case of preexistent thrombophilia status, herein a G20210A prothrombin gene mutation.
We have previously reported a similar observation in a 40-year-old woman with splenic venous infarction and thrombosis, hyperhomocysteinemia associated with a cobalamin deficiency related to celiac disease, and a preexistent thrombophilic disease: a C677T methyltetrahydrofolate reductase gene mutation.2–
In our opinion, the question as to whether cobalamin deficiency may favor the onset of venous thrombosis remains questionable. We have previously reported a retrospective study of a cohort of patients (n = 120) with moderate hyperhomocysteinemia (20 ± 9 μmol/L; extreme, 13 to 42 μmol/L) related to cobalamin deficiency (145 ± 37 pmol/L; extreme, 45 to 200 pmol/L).3–
In our study, we have observed 2.5% of venous thrombosis (all deep venous thrombosis and pulmonary embolism) in the group of patients with hyperhomocysteinemia related to cobalamin deficiency vs 2.6% in a control group (p value not significant).4
We suggest that future studies should be undertaken to definitively link hyperhomocysteinemia and cobalamin deficiency to venous thrombosis.
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